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Clinical benefit of angiotensin-converting enzyme inhibitors in chronic heart failure
W Kiowski1, G Sütsch, L Dössegger
1Division of Cardiology, University Hospital, Zürich, Switzerland.
Insights
Angiotensin-converting enzyme (ACE) inhibitors effectively treat chronic heart failure by improving symptoms, slowing left ventricular dysfunction, and reducing mortality. These benefits suggest ACE inhibitors may also stabilize atherosclerosis.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Chronic heart failure management aims to reduce congestion, prevent left ventricular dysfunction progression, and decrease mortality.
- Angiotensin-converting enzyme (ACE) inhibitors are a key therapeutic class investigated for these goals.
Purpose of the Study:
- To review the evidence supporting the use of ACE inhibitors in chronic heart failure.
- To evaluate their impact on symptoms, disease progression, mortality, and potential effects on atherosclerosis.
Main Methods:
- Meta-analysis of randomized controlled trials.
- Review of major clinical trials (e.g., SOLVD, CONSENSUS I, SAVE).
- Analysis of symptomatic improvement, left ventricular function, mortality rates, and reinfarction incidence.
Main Results:
- ACE inhibitors significantly improve exercise tolerance and reduce heart failure symptoms, a likely class effect.
- Demonstrated benefit in slowing the progression of left ventricular dysfunction.
- Ample evidence supports mortality reduction across various patient populations, including post-myocardial infarction.
- Potential role in stabilizing atherosclerotic disease, though not fully understood.
Conclusions:
- ACE inhibitors are crucial for managing chronic heart failure, offering symptomatic relief, improved ventricular function, and reduced mortality.
- Further research is warranted to elucidate the mechanisms behind ACE inhibitors' potential cardioprotective and anti-atherosclerotic effects.
Abstract:
The ideal therapy for patients with chronic heart failure should reduce symptoms related to pulmonary congestion or low perfusion, prevent the progression of left ventricular dysfunction and, ultimately, should reduce mortality. Extensive studies in humans have investigated the effects of angiotensin-converting enzyme (ACE) inhibitors on these goals of therapy. As an example, the ACE inhibitor cilazapril significantly improved exercise tolerance, as borne out by a meta-analysis of six placebo-controlled, randomized 3-month trials. Comparison of the effects of cilazapril and captopril vs. placebo in one of the trials documented similar improvement in exercise tolerance (14 vs. 17%). Results from other randomized comparative trials suggest that the improvement in symptoms represents a class effect of ACE inhibitors. A beneficial effect of ACE inhibition on the progression of left ventricular dysfunction has also been demonstrated in the SOLVD trial, and a reduction of mortality has been amply documented in several mortality trials (CONSENSUS I, SOLVD, V-HeFT-II, SAVE, AIRE, SMILE) in patients with or without preceding myocardial infarction. Reports that ACE inhibitors also reduce the incidence of reinfarction after myocardial infarction have not been confirmed in all studies but raise the interesting concept that ACE inhibition may interact, in a beneficial but thus far not well-understood way, with key processes in the development of atherosclerosis, thereby preventing plaque rupture, thrombus formation, and myocardial infarction. Taken together, a large database convincingly demonstrates that ACE inhibitors are effective not only in improving symptoms but also in the prevention of progression of left ventricular dysfunction, in the reduction of mortality, and possibly in stabilizing the atherosclerotic disease process.